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Article Type: Commentary | DOI: 10.36502/2020/hcr.6169 | J Health Care and Research. 2020 Jul 31;1(2):119-24
Halim M1*, Halim A2
Corresponding Author: Michael Halim Address: University of Salford, MSc Biomedical Science, Greater Manchester, United Kingdom; Email: email@example.com Received date: 16 June 2020; Accepted date: 18 July 2020; Published date: 31 July 2020
Citation: Halim M, Halim A. Commentary: The Effects of Inflammation, Aging, and Oxidative Stress on the Pathogenesis of Type II Diabetes. J Health Care and Research. 2020 Jul 31;1(2):119-24.
Copyright © 2020 Halim M, Halim A. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Keywords: T2DM, Inflammation, Oxidative Stress, Ageing, Pathogenesis, Pancreatic Beta Cells, Insulin Signalling, Insulin Resistance
Type II Diabetes Mellitus (T2DM) is a high-risk metabolic condition associated with high mortality due to hyperglycemia. Many studies have focused on how inflammation, aging, or oxidative stress influences the pathogenesis of T2DM. The functional anomalies of the pancreatic beta cells attribute to insulin resistance which is the primary cause of T2DM manifestations and complications. This is evidenced in polymorphism in the TNF-α gene which inhibits insulin production, metabolism, and utilization during T2DM development. The dysregulation of insulin signaling involves multiple pathways. Various factors such as epigenetics, oxygen radicals, and glucolipotoxicity are implicated in the pathogenesis. Low-grade inflammation mediated by pro-inflammatory cytokines and chemokines such as interleukin-1 attack peripheral tissues and mediates the activation of critical pathways involved in T2DM pathogenesis via transcriptional factors. The core factor resulting in inflammation is hyperglycemia. The result is the release of inflammatory mediators which then affect neurons in the nervous system and alter microvascular and enzymatic pathways to elicit severe complications such as neuropathy. Oxidative stress and inflammation share an intertwined relationship in the pathogenesis of T2DM. High levels of reactive oxygen species increase the level of DNA damage markers and expose pancreatic beta-cell lines to dysregulation through reduced expression of the insulin gene. The link between the interaction of oxidative stress and inflation in the human body increases the level of interleukin-6 which triggers superoxide radicles and oxidative stressors increase which have been shown to affect free fatty acids metabolism inversely Finally, the aspect of cellular senescence in adipocytes and pancreatic beta cells explain why age is a critical factor in T2DM pathogenesis. Overall, the three factors discussed have a crucial role in T2DM disease states, progressions, and complications.